Intraocular lens (IOL) malposition may range from simple decentration to frank luxation of the IOL into the vitreous. The displaced IOL (the so-called "dropped lens syndrome") may chafe against adjacent tissues, causing complications such as chronic uveitis, cystoid macular oedema, glaucoma, retinal detachment, epiretinal membrane, and visual axis obstruction. We recently received a pseudophakic human eye obtained postmortem from a case of dropped lens syndrome. This allowed us to document histopathologic profiles of several undesired sequelae caused by failed cataract surgery-IOL implantation procedure. We termed this entity "bipseudophakia", due to the presence of both posterior chamber (PC) and anterior chamber (AC) IOLs. The PC IOL had dislocated into the vitreous cavity after a faulty phacoemulsification procedure and the one haptic of the AC IOL had protruded into an iridectomy.
A 95-year-old Caucasian patient had undergone phacoemulsification in the left eye with attempted implantation of a one-piece all polymethyl methacrylate (PMMA) PC IOL in August 1992. The procedure was complicated by intraoperative rupture of the posterior capsule, leading to dislocation of the IOL into the vitreous cavity. The surgeon attempted unsuccessfully to remove the dislocated IOL from the posterior segment. A second attempt to achieve pseudophakia was made in March 1993, eight months after the initial procedure. An IOLAB 85J, four-point fixation Kelman multiflex design was placed in the anterior chamber, without removing the PC IOL. In August 1996, three years after the second surgery, the patient underwent an ophthalmological examination because of pain in the left eye. At that time, the best-corrected visual acuity (BCVA) of this eye was 6/36. Slitlamp examination revealed corneal decompensation. The posterior segment could still be assessed and no abnormalities were observed. In October 1996, the visual acuity in the affected eye decreased to 6/60 due to marked corneal decompensation and the intraocular pressure (IOP) measured 21 mmHg. Penetrating keratoplasty measured recommended, but the patient chose not to have the procedure. In subsequent examinations the visual acuity progressively decreased to finger counting while the IOP increased to 31 mmHg. The patient was treated with a 0.5% solution of timolol maleate. The last known examination was done in December 1999, seven years after the second procedure. At that time the slitlamp examination showed epithelial and stromal corneal oedema with vascularisation. The patient still refused penetrating keratoplasty.
Following the patient's death in October 2000 the eyes were enucleated, forwarded to our Centre and placed in 10% neutral buffered formalin. Gross examination of the anterior segment (from an anterior or surgeon's view) after excision of the cornea revealed the ACIOL fixated in the 6-12 o'clock meridian [Figure - 1a]. The upper haptic was displaced into the iridectomy at 12 o'clock [Figure - 1b]. Examination of the globe from the Miyake-Apple posterior view revealed a large Soemmering's ring containing large amounts of residual cortical material [Figure - 1c]. A large tear of the posterior capsule was noted. One haptic of the PCIOL had broken away from the remainder of the luxated lens and was sandwiched between the ciliary body and the capsular bag at 7 o'clock. Gross examination of the posterior segment did not show any retinal tears. The PC IOL (without the broken haptic) was situated in the vitreous at 6 o'clock, in the region of the ora serrata [Figure - 1d]. It did not appear to be securely adherent to adjacent tissues and was movable.
Histological sections of the cornea, anterior and posterior segments were prepared and stained with hematoxylin-eosin, periodic acid-Schiff (PAS) and Masson's trichrome. The corneal epithelium was thinned and atrophic secondarily to destruction by long standing oedema. The corneal epithelium and the underlying Bowman's layer and the stroma were separated by an ingrowth of fibrovascular tissue. The Bowman's layer was partially destroyed. The Descemet's membrane was intact and thickened with marked endothelial cell loss, with only a few cells visible in some sections [Figure - 2a]. The imprint of one haptic of the AC-IOL into the angle recess is shown in [Figure - 2b]. A moderate posterior tuck of the iris and formation of Masson's trichrome-positive fibrotic tissue at the point of haptic contact [Figure - 2b] was noted. The ganglion cell layer and nerve fibre layer had also atrophied from long-standing glaucoma. A thin epiretinal membrane was noted at the midperiphery of the retina [Figure - 2c]. The macula showed early cystoid macular oedema observed as a thickening of the outer plexiform layer and an accumulation of fine transudates within the outer plexiform layer [Figure - 2d]. The optic nerve showed atrophy with gliosis, thickening of pial septae and cystoid (swiss cheese) spaces in the optic nerve parenchyma.
Dislocation of an IOL into the vitreous is a rare complication and its frequency has been reported to range between and 0.2% to 1.8%. Posteriorly dislocated IOLs have been reported to be well tolerated in many eyes. Long-term observation has shown that dislocated IOLs could remain in the vitreous for a long time without serious complications, if vitreous surgery is not possible. Laganovska and Roider described 6 patients with dislocated IOLs in the vitreous. One patient was followed up for 6 years, two patients for 3 years, two patients for 2 years and one patient for 1 year. In all cases, the retina remained attached and the IOP was below 20 mmHg. In 2 of 6 patients, second IOL was implanted into the anterior chamber without explantation of the posteriorly dislocated IOL. The best corrected visual acuity (BCVA) in the patients with secondary AC-IOL implantation was 6/15 and 6/18 respectively.
To the best of our knowledge detailed histological features of a posteriorly dislocated IOL in the vitreous have not been previously reported. This report of "bipseudophakia" provides a unique clinicopathological demonstration of several possible deleterious sequelae of two less-than-perfect IOL implantation operations. The large Soemmering's ring was present because the surgeon in the initial procedure had to halt the aspiration steps due to capsule rupture with subsequent dislocation of the IOL. This raises the question as to whether we should continue the lens implantation when encountering a large posterior capsule defect and if implantation is chosen, which lens and what technique should be used? Assuming the corneal and filtration structures were undamaged, the placement of an open-loop AC-IOL intraoperatively as done here, or later in the postoperative period is an option. The second option would be the use of various sutured PCIOL techniques. These procedures are much more difficult to perform than is insertion of an ACIOL so these are best done by specially trained surgeons. The third option would be implantation of an iris claw IOL.
Various surgical techniques have been suggested for removal of dislocated IOLs from the vitreous. Nevertheless, these may be complicated in the presence of a second IOL. Paulmann et al., in their report of a case of intraoperative dislocation of a PC IOL into the vitreous cavity implanted a second IOL in the ciliary sulcus during the same procedure. Forty-one days after cataract surgery the dislocated IOL was removed by pars plana vitrectomy, but this was complicated by retinal detachment.
In summary, the case reported here illustrates the possible clinicopathological findings related to complications of ACIOL implantation and posterior dislocation of PCIOLs, and highlights the specific deleterious sequelae of failed cataract surgical-IOL procedure.
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